Bibliothek

Notizen: Summary The role of kinins as mediator substances is increasingly recognized in cerebral ischemia and trauma. It has previously been shown that cerebral exposure to bradykinin, which causes brain edema, is associated with arteriolar dilation and selective opening of the blood-brain barrier (BBB) to small molecular weight indicators, such as Na+-fluorescein. Since the evidence suggests that these effects results from an activation of the arachidonic acid cascade, particularly from formation of E- and I-type prostaglandins, therapeutical inhibition of the cerebral effect of bradykinin has been attempted by pretreatment of experimental animals with dexamethasone. The BBB function and changes of the pial vessel diameters were studied by fluorescence microscopy in cats in alphachloralose anesthesia during superfusion of the exposed cerebral cortex. After a control phase bradykinin was added to a cerebral superfusate in concentrations of 4×10−8 M to 4×10−3 M. Two additional groups of animals received dexamethasone in a dose of 1, or 5 mg/kg body wt., respectively, 5h prior to the cerebral superfusion with bradykinin. Na+-fluorescein (mol wt.: 376) was infused intravenously as a BBB indicator. The BBB marker remained strictly confined to the intravascular compartment under control conditions. Pretreatment with dexamethasone did not prevent opening of the BBB by bradykinin, either at the low, or high dose. However, the low dose of dexamethasone blunted the vasodilatory response to bradykinin, whereas the high dose (5 mg/kg) was found to enhance the dilatory properties of bradykinin at concentrations of 4×10−3 M. Further, dexamethasone at 1 or 5 mg/kg was observed to facilitate dilation of the pial veins upon superfusion with bradykinin, whereas a moderate decrease of venous diameter to bradykinin was observed in untreated controls. Taken together, the current experiments demonstrate that dexamethasone does not prevent opening of the BBB by cerebral administration of bradykinin, whereas it markedly influences vasomotor responses induced by the peptide.

Notizen: Summary The effect of reversible cerebral ischaemia on brain oedema development was studied with a gravimetric method. Cerebral blood flow changes after ischaemia were correlated with alterations in brain specific gravity. Forebrain ischaemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The specific gravity of different brain structures was determined in a Percoll® column up to 24 h after ischaemia. In addition, regional cerebral blood flow was measured by14C-iodoantipyrine autoradiography. Cerebral ischaemia resulted in reduction of cerebral blood flow to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischaemia blood flows were still reduced to 30–50% of the control level indicative of delayed postischaemic hypoperfusion. Specific gravity in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischaemia, and was still significantly reduced at 1 h, while it was normal again 6 hrs later. Regression analysis between regional cerebral blood flows and the corresponding specific gravities were made at various time points, but no significant correlations could be established. Other mechanisms, like vasoconstriction, rheologic or metabolic factors may be causative for the delayed postischaemic hypoperfusion.

Notizen: Summary Local cerebral blood flow (1CBF) was measured autoradiographically 60 minutes after 15 minutes of forebrain ischaemia in rats treated with superoxide dismutase (SOD) before (50 mg · kg−1 body weight) or at the end of the ischaemia period (4mg·kg−1 body weight). Incomplete forebrain ischaemia was produced by a combination of common carotid artery occlusion and bleeding to a mean arterial blood pressure of 50 mmHg. During ischaemia the 1CBF values in cortical areas were less than 3% of the preischaemic values and treatment with SOD prior to ischaemia did not influence 1CBF during ischaemia. Sixty minutes after termination of cerebral ischaemia the 1CBF values were decreased to between 40 and 60% of values found in control animals. Neither form of treatment improved the postischaemic cerebral blood flows. The results imply that postischaemic flow disturbances in the brain may not be due to extracellular superoxide production.

Notizen: Summary Severe head injury is frequently associated with focal or global disturbances of cerebral blood flow and metabolism. Routine monitoring of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in these patients does not provide information about critically reduced local or global cerebral blood flow. Measurements of cerebral lactate difference, Lactate-Oxygen-Index (LOI) and cerebral oxygen extraction were evaluated for advanced monitoring by comparing these parameters with ICP, cranial computed tomography (CCT) findings, and outcome in a group of severely head-injured patients. In 21 patients with severe brain trauma (GCS ⩽8), arterial as well as jugular venous lactate levels and oxygen saturation were measured in vitro every 6 h after admission of patients to the intensive care unit (ICU) throughout the acute course of treatment. Arterial blood pressure, blood gases, and ICP were assessed by standard monitoring measurements. CCT was performed initially after admission of the patients to the hospital, during the acute period in the ICU, if indicated, and 10 to 14 days after trauma. Outcome was classified according to the Glasgow outcome scale (GOS) at six months after injury. Data were averaged in each patient for every day after trauma and over the entire monitoring period. Resulting values were tested for correlation by regression analysis. Additionally, the data of the group of patients with normal to minimally elevated mean ICP (ICP〈20 mmHg, n=12) were compared to those of the patients with increased mean ICP (ICP〉20 mmHg, n=9). The cerebral lactate difference in all patients on the day of trauma was significantly increased as compared to the later period (0.20 vs. 0.11-0.07 mmol/L, p〈0.05), but was not different with high or normal to minimally elevated ICP. In patients with intracranial hypertension, the cerebral lactate difference remained significantly increased from the first to the fifth day after injury, whereas it normalized in this period in the group with normal to minimally elevated ICP. Averaged over the acute course, patients with increased ICP had significantly higher mean lactate differences (0.18±0.16 vs. 0.067±0.025 mmol/L, p=0.001) and higher mean LOIs (0.072±0.071 vs. 0.028±0.013, p=0.011). There was a significant correlation of increased mean cerebral lactate difference to poor outcome (r=0.46, p=0.035). Cerebral oxygen extraction in all patients tended to increase on the day of trauma (36.7% vs. 29.2% to 31.5% during the subsequent course), but this difference was not significant. The initial degree of brain swelling, classified by CCT according to Marshallet al. (1991), showed no correlation with cerebral lactate differences, ICP, O2-extraction, or outcome. Neither was there a correlation of cerebral oxygen extraction to ICP nor to outcome. In conclusion, the severity of brain trauma and outcome of patients was reflected by increased cerebral lactate production. Unchanged values of global cerebral oxygen extraction suggest that the regulatory mechanisms of brain oxygen supply were not impaired by trauma. Measurements of cerebral lactate differences and brain oxygen extraction may contribute to advanced monitoring in severe head injury.

Notizen: Summary  Intracranial pressure monitoring has a key role in the management of patients developing increased intracranial pressure (ICP). We adopted the Camino fiberoptic system for intracranial pressure measurement in 1993 in our neurosurgical department. The aim of this study was to investigate reliability, handling characteristics and complication rate of the Camino intracranial pressure device.  In an eighteen month period, we prospectively investigated 118 patients with intracranial pathology undergoing Camino fiberoptic intraparenchymal or intraventricular ICP monitoring. The assessment of reliability of ICP monitoring according to patients clinical condition, to cranial computed tomography (CCT) findings and ICP waveform was carried out. Position of the probe and intracranial bleeding complications related to probe insertion were confirmed by CCT. Technical complications, as well as infections due to the device, were documented. In vivo recalibration was performed in 22 patients. At the end of the measuring period the drift of the probe was evaluated and the accuracy of the fiberoptic device was measured by performing a two point calibration.  Recordings of intracranial pressure were carried out with 136 Camino devices (104 parenchymal, 32 ventricular) in 118 patients with an average measuring time of 94.1±79.1 hrs. One hundred and fifteen Camino intracranial pressure devices (85.2%) demonstrated reliability according to the predetermined clinical parameters. The actual mean drift after removal of the devices was 3.4 mmHg±3.2 with an actual daily drift of 3.2±17.2 mmHg. Recorded complications included infection (0.7%), intraparenchymal haematoma (5.1%), and a high complication rate (23.5%) with regard to technical aspects. The Camino intracranial pressure system offers reliable ICP measurements in an acceptable percentage of devices, and the advantage of in vivo recalibration. The high incidence of technical complications identifies a need for improvement in the fiberoptic cable and the fixation system.

Notizen: Summary Leucocytes play an important role in inflammation and immunologic responses. They might be of special significance under pathophysiological conditions of the brain i.e. ischaemia or stroke. It has been shown that neutropenic animals undergoing reversible ischaemia show higher post-ischaemic blood flow, suggesting improved post-ischaemic perfusion. In this study it was investigated therefore, whether polymorphonuclear leucocytes contribute to the nerve cell loss in the hippocampus after a reversible period of ischaemia. Rats were made neutropenic with a specific anti-serum against rat polymorphonuclear leucocytes yielding leucocyte counts less than 10% of normal. The animals were then subjected to 15 min reversible forebrain ischaemia. Quantitative histology was performed after a survival period of 7 days. Nerve cell counts in the frontal cortex and in the CA1 and CA3 sectors of the hippocampus did not reveal any differences between neutropenic rats and animals with normal leucocyte counts. From the results it might be concluded that neutrophils do not significantly contribute to the selective post-ischaemic nerve cell damage in the rat.

Notizen: Summary ¶ Background. Investigations have shown an increase of leukocyte-endothelium-interaction in a variety of organs following an ischaemic insult. To elucidate the role of leukocyte-endothelium-interaction following global, cerebral ischaemia the present study was performed. Methods. Global, cerebral ischaemia was induced for twenty minutes by four-vessel-occlusion (PULSINELLI). Leukocyte-endothelium-interaction was studied in the cerebral microcirculation using a rat closed cranial window and intravital microscopy. Leukocytes were stained intravenously using rhodamine 6G. Diameters of pial vessels, leukocyte centreline velocity and number of rolling or adhering leukocytes were determined off-line up to 2 h following global cerebral ischaemia. To confirm these results immunohistochemistry of the brain was performed. Findings. Four-vessel-occlusion induced an iso-electric EEG, venular stasis and minimal rest flow in arterioles. Reperfusion yielded a significant increase of the arteriolar (p〈0.001) and a smaller increase of the venular diameters (p〈0.01). Up to 2 h after ischaemia no significant increase of the number of rolling or adhering leukocytes was measured which was confirmed by immunohistochemistry. Interpretation. In contrast to other studies, in particular regarding focal cerebral ischaemia, an increase of leukocyte-endothelium-interaction in rat brain following 20 min of global cerebral ischaemia was not observed despite histological evidence of ischaemic damage. Thus in our model leukocytes seem not to contribute to the brain damage following global ischaemia.

Notizen: Abstract A new device was developed for rapid assessment of PO2 values in viable tissue, such as the brain, using a multiwire surface electrode. The instrument utilizes a phonograph-like construction with weightless suspension of the electrode which thus minimizes surface pressure and allows for compensation of brain movements. The new and original component of the present device is the motor-driven, servo-controlled rotation of the PO2 electrode around its vertical axis. This enables PO2 measurements from precisely defined locations. From values measured on rabbit brain surface a PO2 histogram was constructed. The mean PO2 and distribution histogram were similar to those obtained with a needle electrode. The novel device, therefore, enables accurate and fast tissue PO2 measurements with minimal risk of brain damage.